Trichinosis is a parasitic disease transmitted to humans predominately by infected pork. This disease causes severe pain and sometimes death to infected individuals. Infection by larvae of the nematode Trichinella spiralis causes dramatic changes in mammalian muscle morphologically, ultrastructurally, and biochemically. Several alterations suggest that infected muscle is suspended in a regenerative muscle phenotype. These include the proliferation of various organelles such as nuclei, mitochondria, golgi apparatus and rough endoplasmic reticulum. However, other alterations such as mitochondrial dysfunctions, and the proliferation of a collagen capsule and lysosomes, which are unlike regenerative muscle, suggest that the parasite actively alters normal host function. Characterizing these alterations, demonstrating the level at which they are regulated, and identifying parasite factors that may be responsible for these changes is important for elucidating 1) the characteristics of the cell that are important for survival of the parasite; 2) the mechanisms responsible for the altered host state; and 3) the role that the larva plays in determining the host phenotype. Attaining these goals could lead to novel methods to prevent transmission of the disease. Since the pathology of trichinosis has similarities to other parasitic and genetic diseases of muscle, obtaining answers to these questions for trichinosis may have application to other muscle diseases. To approach these questions, the hypothesis that T. spiralis infected muscle has a regenerative muscle phenotype which is actively influenced by the parasite will be tested by completing the following specific aims: 1) Determine the state of differentiation of the infected muscle with regard to normal and regenerative muscle. 2) Determine the level at which the expression of the muscle specific protein genes are altered in infected muscle, e.g. transcription, posttranscription or posttranslation. 3) Identify and characterize larval proteins that are located in the host cell.